Omega-3 Fatty Acids of No Benefit in Multiple Sclerosis

Fran Lowry

April 19, 2012

April 19, 2012 — Omega-3 fatty acid supplements failed to reduce disease activity in patients with relapsing-remitting multiple sclerosis (MS), either as monotherapy or in combination with standard immunomodulatory treatment, according to new results of a randomized placebo-controlled trial.

The finding, from the 4-year Omega-3 Fatty Acid Treatment in Multiple Sclerosis (OFAMS) trial, goes against those of preliminary studies that suggested omega-3 supplementation would have a protective effect in MS, lead author Øivind Torkildsen, MD, PhD, from Haukeland University Hospital, Bergen, Norway, told Medscape Medical News.

"It has been estimated that about a third of all MS patients are using or have tried supplementation with omega-3 to control disease progression and neurologists have traditionally recommended omega-3 supplementation to their MS patients," Dr. Torkildsen said. "Although this is the most commonly used and recommended complementary treatment for MS, there have not been any randomized controlled studies to document if omega-3 actually has an effect on MS disease activity."

The OFAMS results were published online April 16 in the Archives of Neurology .

The study was conducted in 13 public neurology departments in Norway from 2004 to 2008 and included 92 patients with active relapsing-remitting MS with a disability score of 5.0 or less on the Kurtzke Expanded Disability Status Scale.

Dr. Torkildsen and his team randomly assigned 46 patients to receive oral omega-3 fatty acids in the form of 1350 mg of eicosapentaenoic acid and 850 mg of docosahexaenoic acid daily, and 46 patients to receive placebo.

After 6 months, all patients additionally received subcutaneous injections of 44 µg interferon beta-1a 3 times per week for another 18 months.

They were followed for 2 years with repeated magnetic resonance imaging (MRI) to measure disease activity according to the number of new T1-weighted gadolinium-enhancing lesions in the brain. Relapse rate, disability progression, fatigue, quality of life, and safety were also measured.

Throughout this time, no positive effect of omega-3 supplementation on any of the measured disease variables was found.

The cumulative number of gadolinium-enhancing MRI lesions during the first 6 months was similar in the omega-3 fatty acids and placebo groups (median difference, 1; 95% confidence interval [CI], 0 - 3; P = .09).

Similarly, there was no difference in relapse rate (median difference after 6 months, 0; 95% CI, 0 - 0; P = .54; median difference after 24 months, 0; 95% CI, 0 - 0; P = .72).

Seventy percent of patients in both study groups had no disability progression (P > .99), and no differences were detected in fatigue or quality-of-life scores. No safety concerns were associated with omega-3 fatty acid treatment. Supplementation did not interfere with interferon-beta treatment.

Findings a Surprise

Dr. Torkildsen admitted he and his group were surprised by the study findings, given preclinical results that suggested a positive effect with omega-3 supplementation. "This shows how important it is to perform controlled studies," he said.

"We hope this study will offer physicians a better basis for giving their patients evidence-based advice on dietary modification in MS. I think doctors should tell their patients that there is no evidence for a positive effect of omega-3 supplementation in MS," Dr. Torkildsen added.

But there is emerging evidence of benefit with vitamin D, he said. "Many sources of omega-3 also contain vitamin D and there is growing evidence that vitamin D supplementation could have a positive effect on MS disease activity."

Commenting on this study for Medscape Medical News, Daniel Kantor, MD, president of the Florida Society of Neurology and the medical director of Neurologique, an organization dedicated to patient-centered care, research, and education in Jacksonville, said the paper was important because many patients with MS are taking supplements without much evidence for their benefit and their potential for harm.

"As neurologists, it is incumbent on us to be familiar with the state of the evidence for various complementary medications," Dr. Kantor, who was not part of the study, said in an interview.

"In this well-designed trial, omega-3 supplementation was not found to be beneficial alone for the first 6 months or in combination with beta-interferon 1a for the remainder of the 2 years," he said.

"There are, however, interesting trends, but not statistically significant. Curiously, the group originally treated with placebo had less gadolinium-enhancing lesions than the omega-3 group, but the opposite was true in terms of T1 hypointensities or black holes. This mismatch could suggest the possibility that omega-3 is actually harmful in terms of inflammation but protective in terms of neurodegeneration," Dr. Kantor said.

This highlights the need for actually studying supplements because they may not always be beneficial, he added.

"In terms of other potential benefits of omega-3 supplementation, there were less people with myalgias in the treated group than the placebo group. This may suggest that there is a role for omega-3 in reducing muscle pains, and potentially in reducing the side effects of interferon beta-1a," he suggested.

The study was funded by the Western Norway Regional Health Authority, Norwegian Multiple Sclerosis Society, Pronova Biocare, Amersham Health, Norway, and Merck Serono, Norway. Dr. Torkildsen reports financial relationships with Merck-Serono, Novartis, and Biogen Idec.

Arch Neurol. Published online April 16, 2012. Abstract

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